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What are 5 congenital defects that lead to a right to left shunt? What is the presentation of a right to left shunt (congenital)? Treatment?

Early cyanosis; blue babies; diagnosed prenatally or become evident soon after

Surgical correction or maintenance of PDA

5 T's

Truncus arteriosus (1 vessel)
Transposition of great vessels (2 switched vessels)
Tricuspid atresia (Tri=3)
Tetralogy of Fallot (4)
TAPVR (5 letters)


What is the pathophys of persistent truncus arteriosus? What usually accompanies it? Pathophys of transposition? What makes it compatible with life? Treatment? Anatomy of tricuspid atresia? What makes it compatible? What causes tetralogy of fallot? What are the 4 anatomical features? Pathophys/symptoms? What does squatting do? How? Treatment? What is TAPVR? What is it associated with?


Failure of aoricopulmonary septum to form

Aorta leaves RV and pulmonary trunk leaves LV
Failure of AP septum to spiral
Must have mixing of blood (VSD, PDA, or PFO)
Surgical intervention within months to prevnt death

Absence of tricuspid vavle and hypoplastic RV
Requires both ASD and VSD

The infundibular septum is moved more over the right atria (anterior) so the pulmonary opening is small and aorta opening is large. It's also moved superior which causes a VSD

Pulmonary infundibular stenosis
RVH (boot shaped heart on CXR)
Overriding aorta

Pulmonary stenosis forces right to left flow across VSD leading to early cyanotic tet spells and RVH.
Squatting incr. SVR which decr. right to left shunt which incr. cyanosis

Early surgical correction

TAPVR-total anomalous pulmonary venous return
Pulmonary veins drain in right heart
ASD and sometimes PDA allow for right to left shunting which maintains CO


What are 3 left to right shunts? How do they present? Order of commonness?

Late cyanosis-blue kids


When does vsd present? What can large lesions lead to? What is heard on auscultation in ASD? What are the symptoms? What does PDA lead to? What is heard on auscultation? What happens if its uncorrected?

Can present after weeks after birth or always be asymptomatic.
LV overload and HF

Loud S1 and wide fixed split S2
No symtoms to HF

Decr. lugn resistance leads to left to right shunt leads to progressive RVH and/or LVH and HF
Continuous machine like murmur
Can lead to late cyanosis in lower extremities


What is the pathophys of eisenmenger syndrome? Symptoms? What are coarctation of the aorta? What is it associated with? symptoms?

left to right shunt leads to incr. pulmonary blood flow leading to remodeling of vasc. leading to pulm. artery hypertension.

RVH occurs to compensate and the shunt becomes right to left

late cyanosis, clubbing, and polycythemia


aortic narrowing near insertion of ductus arteriosus
bicuspid aortic valve, turners
hypertension in upper extremiteis and weak, delayed pulse in lower
Collateral arteries erode ribs (notched appearance on x ray)


What cardiac defects are associated with fetal alcohol syndrome, congenital rubella, DS, infant of diabetic mother, marfan syndrome, prenatal lithium, turners, williams, and 22q11 syndromes?

fetal alcohol syndrome: VSD, PDA, ASD, TOF

congenital rubella: SEPTAL DEFECTS, PDA, pulm. artery stenosis

DS: AV septal defect (endocardial cushion defect), VSD, ASD

infant of diabetic mother: Transposition

marfan syndrome: MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

prenatal lithium: ebstein anomaly

turners: Coarc, bicuspid

williams: supravalvular aortic stenosis

22q11 syndromes: truncus, TOF


What is the definition of hypertension? Risk factors? What is primary hypertension? Relations? Percentage of cases? Secondary? Assocations? What is hypertensive urgency? What is a hypertensive emergency? Symptoms? What does hypertension presdispose to? What is the pathology of fibromuscular dysplasia and hypertensive nephropathy?

Persistent systolic >140 or diastolic >90

Incr. age, obesity, diabetes, inactivity, excess salt, excess alcohol, family history, black>white>asian

90% is primary (Incr. CO or TPR)
10% secondary (fibromuscular dysplasia (beads on a string of renal artery), primary hyperaldosteronism, etc.)

Severe (>180/>120) hypertension without end organ damage

Severe hypertension with end ordgan damage (papilledema, encephalopathy, stroke, retinal hemorrhages and exudates, MI, HF, aortic dissection, kidney injury, MAHA, eclampsia)

CAD, LVH, HF, a fib, aortic dissection, aortic aneurysm, stroke, chronic kidney disease (hypertensive nephropathy--renal artery hyalinosis), retinopathy


What are xanthomas? Where do they occur? What are tendinous xanthomas? What is corneal arcus? What causes them?


Plaques or nodules composed of lipidl aden histiocytes in skin (eyelids=xanthelasma)

Lipid deposit in tendon,especially achilles

liipid deposit in cornea


Describe arteriosclerosis. Describe the two types of arteriolosclerosis. Describe monckeberg arteriosclerosis.

Artery hardening with thickening of wall and loss of elasticity

Small arteries and arterioles
Hyaline: thickening of vessel walls in essential hypertension or diabetes
Hyperplastic: onion skinning in severe hypertension

Medial calcific sclerosis
Medium sized arteries
calcification of elastic lamina leading to vascular stiffening w/o obstruction.
Does not obstruct blood flow


What is atherosclerosis? What are some modifiable and non modifiable risk factors? Describe the pathophys. Complications? Common locations? Symptoms?

Elastic and large and medium sized muscular arteries: arteriosclerosis caused by build up of plaques.

Modifiable: smoking, hypertension, hyperlipid, diabetes
non: age, family history, gender,

Endothelial cell dysfuntion
macrophage and LDL accumulation
Foam cell formation
Fatty streaks
Smooth muscle cell migration (PDGF and FGF)
Smooth cell proliferation
EC matrix deposition
Fibrous plaque
Complex atheromas

Aneurysm, thrombosis, embolism, Periph. vac. disease, ischemia, infarcts

Abdom aorta>coronary>popliteal>carotid

Angina, claudication


What is an aortic aneurysm? symtpoms? What do symptoms mean? What is an abdom aortic aneur associated with? Risk Factors? How does it present? What is a thoracic aortiic aneurysm associated with? Risk factors?

Localized pathologic dilatation of aorta
Abdominal or back pain=sign of leak, imminent rupture, dissection

Atherosclerosis (tobacco, incr. age, male, family history)
palpable pulsatile mass

Cystic medial degeneration
Hyperension, bicuspid aortic, marfans, tertiary syphilis


What is an aortic dissection? Assocations? Presentation? CXR findings? Results?

Longitudinal intimal tear forming false lumen

hypertension, bicuspid aortic, marfans

Tearing chest pain of sudden onset, radiates to back
unequal BP in arms

CXR: mediastinal widening

rupture, pericardial tamponade, and death


What is angina? What causes the 3 different types? Triggers? What makes the better? Treatment? Lab findings? Symptoms?

Chest pain due to ischemic myocardium de to coronary artery narrowing or spasm. No necrosis

Stable: Pain during exertion, ST depression on ECG, resolves with rest of Nitroglycerin

Variant (prinzmetal): at rest due to spasm. transient ST elevation. Tobacco, cocaine, and triptans, unknown.
CA channel blockers, nitrates and smoking cessation

Unstable: thrombosis wit incomplete occlusion. May or may not have ST depression and T wave inversion. No biomarkers. Is an increase in frequency or intensity of the angina or when pain occurs at rest.


What is coronary steal syndrome? Describe the pathophys. What is this principle used for?

Distal to coronary artery stenosis, vessels are maximally dilated. Therefore, when a vasodilator is given, they can dilate anymore, so the unstenosed vessels dilate making the stenosed area more ischemic

Pharmacological stress tests


What is sudden cardiac death? Cause? associations? What is chronic ischemic heart disease?

Death from cardiac causes under 1 hour of onset of symptoms.

Arrhythmia (v fib)

CAD, cardiomyopathy, hereditary ion channelopathies

Progressive onset of HF over many years due to chronic ischemic yocardial damage


What is order of most commonly occluded coronary arteries? What are the sytmpoms of MI? What is the gross pathology and microscopic pathology at 0-4 hr, 4-24 hr, 1-3 days, 3-14 days, and 2 weeks to several months?


diaphoresis, N/V, retrosternal pain, pain in left arm and jaw, SOB, fatigue

G: none
M: none

G: dark mottling, pale with tetrazolium stain
M: early coag necrosis, necrotic contents into blood; edema, hemorrhage, wave fibers, neutrophils appear, reperfusion injury? (contraction bands)

1-3 days
G: hyperemia
M: extensive coag necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils

3-14 days
G: hyperemic border; central yellow brown softening-maximally yellow and soft by 10 days
M: Macrophages, then granulation tissue at margins

2 weeks to several months
G: recanalized artery, gray-white
M: contracted scar complete


What is the gold standard for MI diagnosis in first 6 hours? What changes occur? what is the timeline for cardiac troponin? What is it useful for? What is the timeline for CK-MB? Waht is it useful for? Why?

ECG in first 6 hours
STEMI (transmural infarct)=ST elevation
NSTEMI (subendocardial infarct)=ST depression
hyperacute T waves, T wave inversion
pathologic Q waves or poor R wave progression=evolving or old transmural (STEMI) infarct

Troponin I=rises after 4 hours and is incr. 7-10 days; more specific than toher markers

CK-MB=6-12 hours. Diagnosing reinfarction after acute MI b/ levels return to normal after 48 hours.


What leads will have ST elevations or path. q waves in an infarct in the anteroseptal location? anteroapical? anterolateral? Lateral? Inferior? Which CAs are affected?

anteroseptal location? V1-V2 (LAD)
anteroapical? V3-V4 (distal LAD)
anterolateral? V5-V6 (LAD or LCX)
Lateral? I, aVL (LCX)
Inferior? II, III, aVF (RCA)


What are some complications of an MI? When do they occur and why are they problematic?

arrhythmia; first few days

Post infarction fibrinous pericarditis: friction rub (1-3 days)

LV failure and pulmonary Edema

Cardiogenic shock

Ventricular free wall rupture leading to cardiac tamponade and papillary muscle rupture leading to severe mitral regurg and IV septum rupture leading to VSD (3-14 days post MI)

ventricular pseudoaneurysm formation (contained free wall rupture)=decr. CO, risk of arrhythmia, embolus from mural thrombus (3-14 days)

true ventricular aneurysm: outward bulge during contraction; associated with fibrosis (2 weeks to several months)

Dressler syndrome-autoimmune phenomenon leading to fibrinous pericarditis (several weeks post MI)


How is unstable angina/NSTEMI treated? What else is done for STEMI?

anticoag, antiplatelets, beta blockers, ACE I, NO and morphine (symptom control)

Reperfusion therapy most important (percutaneous coronary intervention preferred over fibrinolysis)


What is the most often etiology of a dilated cardiomyopathy? What are some other etiologies? What are some findings? Treatment? What kind of dysfunciton ensues? Gross/microscopic path?

Idiopathic of familial


Alcohol abuse
wet Beri beri
Coxsackie B virus myocarditis
chronic Cocaine use
peripartum Cardiomyopathy
Doxorubicin toxicity

HF, S3, systolic regurgitant murmur, dilated heart on echo, balloon appearance on CXR

Na restriction, ACEI, beta blockers, diuretics, digoxin, ICD, heart transplant

Systolic dysfunction

sarcomeres added in series (eccentric hypertrophy (longer wall not thicker wall))


What are 60-70% of hypertrophic cardiomyopathy caused by (specificallly)? Association? Symptoms? Findings? Treatment? Dysfunction? Gross/micro path? What is obstructive hypertrophic cardiomyopathy?

familial, autosomal dominant (beta myosin heavy chain)

Friedrichs ataxia

Syncope durig exercise and sudden death in yougn athletes

S4, systolic murmur, maybe mitral regurg

Cessation of high intensity exercise, beta blocker or verapamil. ICD.

Diastolic dysfunction

Ventricular hypertrophy (myofibrillar disarray and fibrosis)

HOCM: septal hypertrophy and systolic anterior motion of mitral valve-->outflow obstruction--->dyspnea/syncope


What are some major causes of restrictive/infiltrative cardiomyopathy? dysfunction? What can be seen on ECG?

sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (young children), loffler syndrome (fibrosis with a prominent eosinophilic infiltrate), hemochromatosis.

diastolic dysfunction

Low voltage ECG


What is heart failure? Symptoms? Signs? compare/contrast systolic/diastolic function and how they effect EF, EDV, and contractility/compliance (causes). What most often causes right HF? 2nd leading cause? What treatments decr. mortality? Help symptoms? improve symptoms and decr. motrality in some patients?

cardiac pump dysfunction--->congestion and low perfusion

dyspnea, orthopnea, fatigue

rales, JVD, pitting edema

Systolic: reduced EF, Incr. EDV, Decr. contractility due to ischemia/MI or dilated CM

Diastolic: preserved EF, normal EDV, decr. compliance due to myocardial hypertrophy.

Right HF from left HF, then from cor pulmonale

ACEI and ARBs, Beta blockers (except in acute decompensated HF) and spironolactone decr. mortality

Thiazide or loop diuretics for symptoms

hydralazine with nitrate therapy improve symptoms and mortality in some patients.


What are 3 symptoms of left heart failure? Pathophys of each? 3 symptoms of right heart failure and pathophys?

Orthopnea: SOB when supine. Incr. venous return exacerbates pul. vasc. congestion

Paroxysmal nocturnal dyspnea: breathless awakening from sleep

Pulm. edema: incr. pulm. venous pressure-->transudation (hemosidern laden macrophages) in lungs. heart failure cells

hepatomegaly (nutmeg liver): incr. central venous pressure, incr. resistance to portal flow

JVD: incr. venous pressure

Periph. edema: incr. venous pressure leading to transudation


Pathophys of HF as well as compensation?

decr. LV contractility leads to pulmonary congestion leading to pulmonary edema

pulm. congestoin also leads decr. RV output leading to periph. edema

Decr. LV contract. also leads to decr. CO leading to incr. RAAS leading to incr. renal na and h20 reabsorption leading to incr. systemic venous pressure leading to periph. edema as well as incr. preload

Decr. CO also leads to incr. sympathetic activity leading to incr. RAAS and incr. LV contractility

Incr. preload and LV contractility lead to compensation, albeit by causing edema.


What are the 4 types of shock? What causes each of them? How do they affect the skin? How do they affect preload, CO, and afterload? Treatment for each? What is systemic inflammatory response syndrome? First sign of shock? End result of shock?


hemorrhage, dehydration, burns

Cold clammy skin

Very decr. preload, decr. CO, incr. afterload

IV fluids


acute MI, HF, valve dysfunction, arrhythmia

cold clammy

incr. preload, very decr. CO, incr. afterload

inotropes, diuresis


cardiac tamponade, PE

cold clammy

incr. preload, very decr. CO, incr. afterload

relieve obstruction


sepsis, CNS injury, anaphylaxis

warm, dry

decr. preload, incr. CO, very decr. afterload

pressors and IV fluids

SIRS (>=2: fever/hypothermia, tachycardia, tachypnea, leukocytosis/leukopenia

First sign of shock=tachycardia

MODS is end result


What are the symptoms of bacterial endocarditis? What microbe causes acute endocarditis? Subacute? Which is present in colon cancer? Which presents on prosthetic valves? What are some non bacterial causes? IV drug abuse causes? culture negative causes?


Roth spots (white spots on retina surr. by hemorrh.)
Osler nodes (tender raised lesion on finger or toe pads)
Murmur (new onset)
Janeway lesions (painless red lesions on palm or sole)
Nail-bed hemorrhage

acute: staph aureus-rapid onset
subacute: viridans streptococci

Strep bovis: colon cancer
S. epidermidis: prosthetic valves

Non bacterial: malignancy, hypercoag state, lupus

IV=tricuspid=staph, pseudomonas, candida

Culture neg=coxiella burnetii, bartonella spp., HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)


What heart valves are affected in RF (common)? Early lesion? Late lesion? What are aschoff bodies? anitschkow cells? what is the pathophys? Treatment?


early: mitral regurg
late: mitral stenosis

Aschoff: granules with giants cells
anitschkow cells: enlarge macrophages with ovoid wavy rod like nucleus

Immune mediated (type II): antibodies to m protein attack self antigens



How does acute pericarditis prsent? How is it relieved? Auscultation ECG changes? Causes?

sharp pain, aggravated by inspiration
relieved by sitting up and leaning forward

Friction rub

Diffuse ST segment elevation and/or PR depression

idiopathic (viral), confirmed infection (cocsackievirus), neoplasia, autoimmune (SLE, RA), uremia, acute STEMI/Dressler, radiation therapy


What is cardiac tamponade? Results? Findings? What is pulsus paradoxus? when is it seen? ECG?

compression of heart by fluid in pericardial space-->decr. CO
Equilibration of diastolic pressures in all 4 chambers

Beck triad (hypotension, distended neck veins, distant heart sounds), incr HR, pulsus paradoxus (decr. in amplitude of systolic BP by >10 mmHg during inspiration-tamponade, asthma, obstructive sleep apnea, pericarditis, croup)

ECG: low voltage QRS and electrical alternans (swinging movement of heart)


What is the pathophys of syphilitic heart disease? Location? gross Appearance? Results?

tertiary syphilis affects the vasovasorum or the aorta leading to atrophy of vessel wall and dilatation of aorta and valve ring

calcification of aortic root and ascending aortic arch. Tree bark appearance.

Aneurysm of ascending aorta or aortic arch; aortic insufficiency.


What is the most common heart tumor? Most common primary in adults? Most common primary in children? Describe them. Location. symptoms. associations. What is kussmall sign? explain pathophys. causes?


Myxoma: adults. 90% in atria. Ball valve obstruction leading to multiple syncopal episodes. Diastolic tumor plop

Rhabdomyomas: children (tuberous sclerosis)

Kussmaul: incr. in JVP on insp. instead of a decr.
Normally, the JVP would decr. because of neg. IT pressure leading to greater filling of the heart. However, if the side of the heart isn't able to fill, the JVP accepts the extra blood that should be going into the heart.

Constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors


What is an angiosarcoma? Locations? Age? Associations? Hepatic angiosarcoma associations? Prognosis? What is bacillary angiomatosis? Cause? epidemiology? Diagnosis? What is a cherry hemangioma? prognosis? What is a cystic hygroma? Association? What is a glomus tumor? Origin? What is kaposi sarcoma? Locations? Assocations? Diagnosis? What is a pyogenic granuloma? symptoms? Associations? What is a strawberry hemangioma? Presentation? prognosis?

Angiosarcoma: head, neck, breast; elderly; sun exposed areas, radiation therapy, chronic postmastectomy lymphedema; hepatic; vinyl chloride and arsenic; very aggressive, difficult to resect due to delayed diagnosis

bacillary: benign capillary skin papules; HIV and B. henselae. Mistaken for kaposi, but has neutrophilic infiltrate

cherry hemangioma: benign capillary hemangioma of elderly; does not regress, incr. in frequency with age

Cystic hygroma: cavernous lymphangioma of neck; turners

glomus tumor: benign, painful red blue tumor under fingernails. modified SM cells of thermoreg. glomus body

Kaposi: endothelial malignancy most commonly of skin, but mouth, GI, and resp. tract; HHV-8 in HIV pts; mistaken for bacillary but has lymph. infiltrate

Pyogenic granuloma: Polypoid capillary hemangioma that can ulcerate and bleed; trauma and pregnancy

Strawberry hemangioma: benign capillary hemangioma of infancy; first weeks of life; grows rapidly and regresses by age 5-8.


What is raynauds phenomenon? Presentation? Location? What is raynauds disease? syndrome? Associations? Treatment?

decr. blood flow to skin due to arteriolar vasospasm in response to cold or stress

white (ischemia) to blue (hypoxia) to red (reperfusion)

Fingers and toes


syndrome: association to a disease such as MCTD, SLE, or CREST.

Ca channel blockers